Rodent Parasite Data for the Sevilleta National Wildlife Refuge, New Mexico (1990-1998)

The 100,000 ha Sevilleta National Wildlife Refuge (SNWR) in central New Mexico lies in a transition zone that straddles several major biomes of the Southwest, including Great Basin Shrub-Steppe, Mogollon Pinon-Juniper Woodland, Great Plains Grassland and Chihuahuan Desert. During 9 years, (1990-1998), collaborating with the University of New Mexico\u27s Long Term Ecological Research (LTER) program, 3,235 rodents (28 species in 4 families) were collected and identified from permanent collecting sites on the 3 major habitat types (grassland, desert/creosote, woodland) on the SNWR. Hosts were necropsied for endoparasites (protozoa [coccidia], helminths) and some ectoparasites. We identified and analyzed all the parasites found in these hosts. By 1998, we had in place the means to easily identify and moniter the parasites from all mammalian hosts caught on the LTER Phase II grant.This is not just another parasite survey; the data we collected was unique for several reasons: 1) This was the first complete inventory of a natural assemblage of parasites from all mammalian (rodent) hosts in 3 different communities, each from a distinctly defined geographic locality (habitat type) over the period of a decade, and beyond; 2) This study was part of a multidisciplinary approach to address conceptual issues of climate change on ecosystem structure and function at multiple scales (individuals, communities, etc) and correlative data from these related studies will strengthen and contribute to the robustness of this data set; 3) As the only parasite study on any of the LTER projects nationwide, it provided an ideal model, and perhaps incentive for parallel longterm studies of parasite communities to be examined in a variety of other habitat types, and from a variety of different perspectives, and other LTER sites in the network.Upon completing the work, we were able to use these long-term data to try to understand the dynamics of natural host-parasite assemblages. Hypotheses were then erected to test/address at least these questions: How do the different parasite communities colonize, mature, climax and senesce over time (or do they?), Do they vary in response to abiotic (climate change) and/or biotic (dispersal, colonization) factors? What temporal and spatial scales, and among what kinds of organisms, do coevolutionary processes influence the community organization of these parasites? Studies of the dynamics of multiple, coexisting species are confined primarily to microtine rodents and have hinted that multiannual cycles tend to be synchronous (Brown and Heske 1990). Are similar patterns seen for the parasites of our desert rodents? Answers to these questions relating to community structure, as well as to questions concerning parasite biodiversity on the SNWR, can be answered paritially or completely by the information we gathered on the parasite species infecting rodents collected on the SNWR. Initial emphasis of our work was on identifying all the parasites collected, by processing 8 consecutive years of parasite data, and on training the undergraduate and graduate students involved in the art of taxonomy and nomenclature of parasitic protozoans and helminths, to supply some of these answers

Are long chain acyl CoAs responsible for suppression of mitochondrial metabolism in hibernating 13-lined ground squirrels?

Hibernation in 13-lined ground squirrels (Ictidomys tridecemlineatus) is associated with a substantial suppression of whole-animal metabolism. We compared the metabolism of liver mitochondria isolated from torpid ground squirrels with those from interbout euthermic (IBE; recently aroused from torpor) and summer euthermic conspecifics. Succinate-fuelled state 3 respiration, calculated relative to mitochondrial protein, was suppressed in torpor by 48% and 44% compared with IBE and summer, respectively. This suppression remains when respiration is expressed relative to cytochrome c oxidase activity. We hypothesized that this suppression was caused by inhibition of succinate transport at the dicarboxylate transporter (DCT) by long-chain fatty acyl CoAs that may accumulate during torpor. We predicted, therefore, that exogenous palmitoyl CoA would inhibit respiration in IBE more than in torpor. Palmitoyl CoA inhibited respiration ~70%, in both torpor and IBE. The addition of carnitine, predicted to reverse palmitoyl CoA suppression by facilitating its transport into the mitochondrial matrix, did not rescue the respiration rates in IBE or torpor. Liver mitochondrial activities of carnitine palmitoyl transferase did not differ among IBE, torpor and summer animals. Although palmitoyl CoA inhibits succinate-fuelled respiration, this suppression is likely not related exclusively to inhibition of the DCT, and may involve additional mitochondrial transporters such as the adenine-nucleotide transporter